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首页> 外文期刊>Journal of Virology >Genetic studies on capsid-length determination in bacteriophage T4. II. Genetic evidence that specific protein-protein interactions are involved.
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Genetic studies on capsid-length determination in bacteriophage T4. II. Genetic evidence that specific protein-protein interactions are involved.

机译：胶囊长度测定的遗传研究噬菌体T4。 II。涉及特定蛋白质 - 蛋白质相互作用的遗传证据。

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摘要

A bacteriophage T4 mutation (ptg19-80c) located in gene 23, which encodes the major structural protein of the T4 capsid, results in the production of capsids of abnormal length. Mutations outside gene 23 which partially suppress ptg19-80c have been described in the accompanying paper (D. H. Doherty, J. Virol. 43:641-654, 1982). Characterization of these suppressors was extended. A complementation test suggested that the suppressors were in genes 22 and 24. These genes coded for the major component of the morphogenetic core of the capsid precursor and the vertex protein of the capsid, respectively. The suppressor mutations were found to have no obvious phenotype in the absence of ptg19-80c. Suppression was shown to be allele specific: other ptg mutations at different sites in gene 23 were not suppressed by the suppressors of ptg19-80c. These results indicated that specific interactions among the three proteins gp22, gp23, and gp24 may play a role in the regulation of T4 capsid-length determination. Current models for capsid-length determination are considered in the light of these results.
机译：位于基因23中的噬菌体T4突变（PTG19-80C），它们编码了T4衣壳的主要结构蛋白，导致产生异常长度的衣壳。部分抑制PTG19-80C的基因23的突变已在伴随的纸张中描述（D.H.Toherty，J.Virol。43：641-654,1982）。延长了这些抑制剂的表征。互补试验表明抑制剂在基因22和24中。这些基因分别编码了衣壳前体的形态发生核和衣壳的顶点蛋白质的主要成分。发现抑制剂突变在没有PTG19-80℃的情况下没有明显的表型。显示抑制是等位基因特异性：PTG19-80C的抑制剂，基因23中不同位点的其他PTG突变不抑制。这些结果表明，三种蛋白质GP22，GP23和GP24之间的特异性相互作用可能在T4衣壳长度测定的调节中起作用。鉴于这些结果，考虑了用于衣壳长度测定的当前模型。

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    《Journal of Virology》 |1982年第2期|共9页
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    D H Doherty;

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  • 收录信息 美国《科学引文索引》(SCI);
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